<Originals>Effects of the prenatal ochratoxin A exposure on behaviors of rat offspring

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The effects of prenatal ochratoxin A (OCA) exposure on postnatal behavior and function of Jcl : Wistar rat offspring were assessed in two experiments. In Experiment 1,pregnant rats were administered orally with 0.25 or 0.5 mg/kg/day of OCA dissolved in 0.1 M sodium bicarbonate on days 11-14 (A) or 15-18 (B) of gestation. Controls received the vehicle similarly on days 11-18 of gestation. The offspring were examined by preweaning and postweaning behavioral tests. In the preweaning test, the offspring in the 0.25 and 0.5mg/kg-A groups showed significantly lower success rates than controls in surface righting reflex. Those in the 0.5 mg/kg-A and B groups also showed significantly lower success rates in negative geotaxis. In the swimming test, the offspring in all OCA-treated groups had significantly lower scores than controls for body angle, and in the 0.25 mg/kg-A group the scores for swimming direction were significantly lower than those of controls. In postweaning tests, avoidance learning task of the rats in the 0.25 and 0.5 mg/kg-A groups was significantly poorer than that of controls. In order to clarify whether the behavioral alteration in the offspring was due to direct effects on embryos or to the indirect effects on the mothers, neonatal rats were cross-fostered in Experiment 2. Pregnant rats were administered orally with 0 or 0.5 mg/kg/day of OCA on days 11-14 of gestation. In the acquisition of avoidance response, the avoidance rates of OCA-treated offspring were significantly lower than those of either the control offspring fostered by other control mothers or the control offspring fostered by OCA-treated mothers. In the extinction of the avoidance response, OCA-treated offspring showed significantly higher avoidance rates compared with either control offspring fostered by other control mothers or control offspring fostered by OCA-treated mothers. These results indicate that prenatal exposure to OCA produced a delay of early reflex development and learning deficiencies. The doses required to induce behavioral disorders were much lower than that to cause death, gross malformations or growth retardation. These behavioral effects were more pronounced during mid-organogenesis (days 11-14) than in late organogenesis (days 15-18), and OCA also produced long lasting impairments of avoidance learning in mature animals. Furthermore, it was demonstrated that learning dysfunctions in the offspring are not of maternal origin but due to the direct effects of OCA on embryos in utero.
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<Originals>Effects of the prenatal ochratoxin A exposure on behaviors of rat offspring

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